Proteomics and Genomics Technology: Comparison in Heart Failure and Apoptosis

Neil J Nosworthy, University of Sydney, New South Wales, Australia
Masako Tsubakihara, University of Sydney, New South Wales, Australia
Cristobal G dos Remedios, University of Sydney, New South Wales, Australia

Abstract

Recent developments in microarray technology in determining the protein and gene content of cellular extracts will allow,
on a much larger scale, the characterization of genes and proteins that change due to heart failure.

Scanned images of 96 gene arrays from Clive and Vera Ramaciotti consortium, University of NSW, Australia. The genes are spotted
in duplicate. Green spots (e.g. actin) indicate genes that are upregulated, orange spots (e.g. tubulin) indicate genes that
are downregulated while yellow spots (e.g. myosin) show genes that have equal expression in donor and diseased hearts. Bright
spots indicate a large amount of gene present, while no color means the gene is absent in the sample.

Figure 2.

Pie chart illustrating a quarter (24×25 spots) of a Micromax gene array in which mRNAs from human left ventricles are compared. The diameter of the pie represents the expression level of each spotted gene (the
stronger the gene expression, the larger the diameter) and dark and light shadings indicate the expression in DCM and donor heart respectively. Equal gene expression divides a pie in half.

Figure 3.

Apoptosis signaling pathways. Upon induction of apoptosis through the Fas signaling pathway, there is an alteration in the
permeability of mitochondrial membranes. This change causes the release of cytochrome c from mitochondria (Mito) into the cytoplasm, which in turn activates cascades of caspases. The Bcl‐2 family of proteins regulates cell death by controlling
mitochondrial membrane permeability.